I have heard that vitamin D may play a role in epilepsy, possibly due to interaction with anti-epileptic drugs.Is this becoming an acknowledged effect?And how much vitamin D is necessary to combat the interaction to reduce seizures?

Response:Epileptic drugs will enhance the destruction of vitamin D making patients who are on anti-seizure medications at higher risk for developing vitamin D deficiency and osteomalacia or rickets.Measurement of 25-hydroxyvitamin D [25(OH)D] is important in patients on antiepileptic medications.Often twice as much vitamin D is required to maintain a blood level of25(OH)D of > 30 ng/ml.Thus, 2,000-4,000 IU of vitamin D/d is usually needed.An alternative is to take 50,000 IU of vitamin D2 either once every week or once every two weeks depending on the serum 25-hydroxyvitamin D level.

MENTAL HEALTH

What is your position on vitamin D and depression and schizophrenia?

Response:There is evidence that vitamin D deficiency during pregnancy increases the risk of the child developing schizophrenia during their adult life.There is also evidence that vitamin D receptors exist in the brain, and that the active form of vitamin D, 1,25-dihydroxyvitamin D, Read more of this article »

It is known that if you are born above 35° latitude at approximately Atlanta, Georgia, and live at this latitude for the first ten years of your life that you have a 100% increase risk of developing multiple sclerosis. Recent studies have suggested that women and men who increase their vitamin D intake above 400 IU of vitamin D a day reduces risk of developing multiple sclerosis by approximately 40%.

It has long been recognized that patients with tuberculous do better when treated with vitamin D or exposed to sunlight. It was recently recognized that the immune cell known as the macrophage needs vitamin D in order to produce a peptide which is responsible for killing infectious agents such as tuberculous. It has been speculated that one of the reasons that influenza occurs in the winter time in tepid climates is because the sun is unable to produce vitamin D, and the resulting vitamin D insufficiency may promote and enhance the infectivity of the influenza virus.

Studies in mice have suggested that pretreating mice that are prone to developing type I diabetes with the active form of vitamin D (1,25-hydroxyvitamin D [1,25(OH)2D]) reduces the development of type I diabetes by 80%. This study is supported by the observation in Finland where children in the 1960’s routinely received 2,000 IU of vitamin D a day during their first year of life. When these children were followed for the next 31 years, it was observed that these children had a reduced risk of developing type I diabetes by 78%. Children who were vitamin D deficient at the same time and also followed for 31 years had an almost 300% increased risk of developing type I diabetes.

The beta islet cells that produce insulin in the pancreas have a vitamin D receptor. The active form of vitamin D stimulates the pancreas to produce insulin. It has been observed that the relative risk of developing type II diabetes is reduced by as much as 33% in men and women who increase their intake of vitamin D above 800 IU/day along with 1,000 milligrams of calcium.

Rickets occurs at approximately six months of age in children who are vitamin D deficient. They can present with growth retardation, skeletal deformities including bowing of the legs or knocked knees, prominent knob like projections along the ribs next to the sternum known as the rachitic rosary and muscle weakness. Infants with vitamin D deficiency also suffer from craniotabes which is a softening of the skull causing it to become square shaped. They can have increase in the bone formation in the front of the head which is known as frontal bossing.

Vitamin D deficiency causes a defect in the ability of the body to deposit calcium into the collagen jello-like matrix in the bone. As a result, the covering on the bone which contains pain sensing nerves is easily deformed resulting in throbbing aching bone pain. Patients with osteomalacia often complain of achiness in their muscles and bones. These non-specific aches and pains in the bones and muscles are often misdiagnoses as fibromyalgia or chronic fatigue syndrome. There have been several studies demonstrating that patients with severe bone and muscle pain and muscle weakness associated with osteomalacia have dramatic improvement in their symptoms when vitamin D deficiency is corrected. It takes months to years to develop osteomalacia and associated symptoms and it takes three to six months before significant improvement in symptoms results from correcting vitamin D deficiency.

Vitamin D deficiency will cause removal of both the calcium and matrix from the bone, and as a result, will cause osteopenia and can precipitate and exacerbate osteoporosis. Unlike osteomalacia which causes bone pain, osteoporosis, which is porotic bone, i.e., holes in the bones and loss of bone does not cause bone pain unless there is an acute fracture. Typically this pain resolves as the fracture heals and can be easily distinguished from osteomalacia.